ArticleFrontiers in molecular neuroscience2022
Differential synaptic mechanism underlying the neuronal modulation of prefrontal cortex, amygdala, and hippocampus in response to chronic postsurgical pain with or without cognitive deficits in rats.
Article in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 7 citations in OpenAlex.
- Review
- Hippocampal Extracellular Matrix Protein Laminin β1 Regulates Neuropathic Pain and Pain-Related Cognitive Impairment.Neuroscience bulletin · 2025Article
- Longitudinal MRI identifies associations between cognitive decline, inflammatory markers, and hippocampal subregion volumes in individuals with knee osteoarthritis.Communications medicine · 2025Article
- Exploring the influence of synaptic density and anxiety on pain perception: evidence from a [11C]UCB-J positron emission tomography imaging study.The international journal of neuropsychopharmacology · 2025Article
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6 authors at 2 institutions in 1 country.
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Abstract
Chronic Postsurgical Pain (CPSP) is well recognized to impair cognition, particularly memory. Mounting evidence suggests anatomic and mechanistic overlap between pain and cognition on several levels. Interestingly, the drugs currently used for treating chronic pain, including opioids, gabapentin, and NMDAR (N-methyl-D-aspartate receptor) antagonists, are also known to impair cognition. So whether pain-related cognitive deficits have different synaptic mechanisms as those underlying pain remains to be elucidated. In this context, the synaptic transmission in the unsusceptible group (cognitively normal pain rats) was isolated from that in the susceptible group (cognitively compromised pain rats). It was revealed that nearly two-thirds of the CPSP rats suffered cognitive impairment. The whole-cell voltage-clamp recordings revealed that the neuronal excitability and synaptic transmission in the prefrontal cortex and amygdala neurons were enhanced in the unsusceptible group, while these parameters remained the same in the susceptible group. Moreover, the neuronal excitability and synaptic transmission in hippocampus neurons demonstrated the opposite trend. Correspondingly, the levels of synaptic transmission-related proteins demonstrated a tendency similar to that of the excitatory and inhibitory synaptic transmission. Furthermore, morphologically, the synapse ultrastructure varied in the postsynaptic density (PSD) between the CPSP rats with and without cognitive deficits. Together, these observations indicated that basal excitatory and inhibitory synaptic transmission changes were strikingly different between the CPSP rats with and without cognitive deficits.
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